Established the first clinical prediction model regarding the risk of hyperuricemia in adult IgA nephropathy.

OBJECTIVE: To construct a novel nomogram model that predicts the risk of hyperuricemia incidence in IgA nephropathy (IgAN). METHODS: Demographic and clinicopathological characteristics of 1184 IgAN patients in the First Affiliated Hospital of Zhengzhou University Hospital were collected. Univariate analysis and multivariate logistic regression were used to screen out hyperuricemia risk factors. The risk factors were used to establish a predictive nomogram model. The performance of the nomogram model was evaluated using an area under the receiver-operating characteristic curve (AUC), calibration plots, and a decision curve analysis. RESULTS: Independent predictors for hyperuricemia incidence risk included sex, hypoalbuminemia, hypertriglyceridemia, blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), 24 h urinary protein (24 h TP), gross hematuria and tubular atrophy/interstitial fibrosis (T). The nomogram model exhibited moderate prediction ability with an AUC of 0.834 (95% CI 0.804-0.864). The AUC from validation reached 0.787 (95% CI 0.736-0.839). The decision curve analysis displayed that the hyperuricemia risk nomogram was clinically applicable. CONCLUSION: Our novel and simple nomogram containing 8 factors may be useful in predicting hyperuricemia incidence risk in IgAN.

Hyperuricemia aggravates the progression of IgA nephropathy.

OBJECTIVE: The relationship between hyperuricemia and IgA nephropathy (IgAN) was evaluated systematically in this research. METHODS: The Preferred Reporting Items for Systematic Review and Meta-analysis statement was employed to design and report the study. RESULTS: Twenty-five studies were included in this meta-analysis with a total of 6048 IgAN patients. The clinical indicators indicated that blood urea nitrogen (BUN) (p < 0.00001, mean difference (MD) = 2.60, 95% confidence interval (CI) 1.74-3.46), serum creatinine (Scr) (p < 0.00001, MD = 44.56, 95% CI 31.15-57.98), diastolic blood pressure(DBP) (p < 0.00001, MD = 3.86, 95% CI 2.84-4.88), systolic blood pressure(SBP) (p < 0.00001, MD = 6.71, 95% CI 4.70-8.71), and 24-h urine protein(24 h TP) (p < 0.00001, MD = 0.76, 95% CI 0.58-0.94) were significantly increased in IgAN with hyperuricemia group than that in normouricemic IgAN group. The pathological analysis indicated that mesangial proliferation (p < 0.00001, MD = 0.12, 95% CI 0.07-0.17), vascular lesion (p < 0.00001, MD = 0.17, 95% CI 0.13-0.20), segmental lesion (p < 0.00001, MD = 0.15, 95% CI 0.03-0.26), tubulointerstitial damage (p < 0.00001, MD = 1.27, 95% CI 1.06-1.48), and glomerulosclerosis (p < 0.00001, MD = 0.56, 95% CI 0.40-0.72) were considerably climbed in IgAN patients with hyperuricemia compared without hyperuricemia group. Additionally, the estimated glomerular filtration rate (p < 0.00001, MD = - 29.03, 95% CI - 36.83 to - 21.23) was decreased in IgAN patients with hyperuricemia compared with normouricemic group. CONCLUSION: Hyperuricemia exacerbates IgAN prognosis through aggravating the clinical outcomes and pathological results of IgAN.